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1

Sekrecyjna fosfolipaza A2 — udział w stresie oksydacyjnym i stanach zapalnych

100%
Chalimoniuk M.
Postępy Biochemii
|
2012
|
tom 58
|
nr 2
2

Nitric oxide synthase and cGMP level in different parts of the brain during aging

63%
Chalimoniuk M., Strosznajder J.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
3

Effect of 7-Nitroindazole on nitric oxide mediated biochemical and morphological alterations evoked by brain ischemia

63%
Chalimoniuk M., Strosznajder J.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
4

Cytozolowa fosfolipaza A2 i jej udzial w chorobie Parkinsona

63%
Stolecka A., Chalimoniuk M.
Postępy Biologii Komórki
|
2008
|
tom 35
|
nr 1
133-146
5

Aged related changes of NMDA receptor mediated nitric oxide depented signaling pathway in brain. Effect of amyloid beta peptides

63%
Chalimoniuk M., Strosznajder J.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
6

Biphasic enhacement of nitric oxide synthase activity and cGMP level following brain ischemia in gerbils

63%
Strosznajder J., Chalimoniuk M.
Acta Neurobiologiae Experimentalis
|
1996
|
tom 56
|
nr 1
7

Receptor mediated second messengers formation and function in aged brain. Modulatory effect of amyloid beta peptides

51%
Strosznajder J., Samochocki M., Chalimoniuk M.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
8

Alteration by aging of phosphoinositides-dependent calcium signalling in brain cortex

51%
Samochocki M., Chalimoniuk M., Strosznajder J.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
9

Astroglia in lead toxicity-neuroprotective or neuro-toxic?

51%
Struzynska L., Sulkowski G., Chalimoniuk M., Lenkiewicz A.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
10

Effect of beta-amyloid peptides on cholinergic receptormediated calcium signaling in brain cortex synaptoneurosomes

51%
Samochocki M., Chalimoniuk M., Strosznajder J.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
11

Modulation of arachidonic acid incorporation into cultured spinal cord neurons

51%
Malecki A., Chalimoniuk M., Trzeciak H. I., Toborek M.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
12

cGMP-dependent protein kinase is involved in MPPplus-induced cytosolic cPLA2 activation in dopaminergic neuronal celi line PC12

51%
Stolecka A., Chalimoniuk M., Langfort J., Strosznajder J. B.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
13

Progressive alteration of the GABA/CLminus channel properties and function during reperfusion time in the hippcampus and the brain cortex

51%
Koladkiewicz I., Samochocki M., Chalimoniuk M., Strosznajder J.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
14

Ischemia-related alteration of GABA A-operated chloride channel properties in gerbil hippocampus and cerebral cortex

51%
Strosznajder J., Koladkiewicz I., Chalimoniuk M., Samochocki M.
Acta Neurobiologiae Experimentalis
|
1998
|
tom 58
|
nr 2
15

Nitric oxide and poly(ADP- ribose) polymerase in signal transduction and neurodegeneration

45%
Strosznajder J., Jesko H., Chalimoniuk M., Zambrzycka A., Strosznajder R.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr Supplement 1
16

Glutamate receptors antagonists attenuate neurological deficits and modulate neuroinflammation in Lewis rat subjected to experimental autoimmune encephalomyelitis

45%
Sulkowski G., Dabrowska-Bouta B., Chalimoniuk M., Lenkiewicz A., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Experimental autoimmune encephalomyelitis (EAE) is an animal model that mimics many aspects of multiple sclerosis (MS). Chronic or relapsing inflammation of the central nervous system results in the destruction of myelin sheath and cytokines play an important role in the pathogenesis of both MS and EAE. Myelin, oligodendrocytes and neurons are lost due to an inflammatory attack by leukocytes infiltrating the central nervous system (CNS) and releasing cytotoxic cytokines, anti CNS antibodies and large amounts of the excitatory neurotransmitter glutamate. Pharmacological studies have suggested that glutamate receptors mediate white matter injury in a variety of CNS diseases, including multiple sclerosis (MS). Memantine and amantadine are ionotropic glutamate receptors (iGluRs) antagonists. Memantine, a clinically applied drug with N-methyl-D-aspartate (NMDA) receptor antagonistic effects, dose-dependently ameliorates neurological deficits in Lewis rats subjected to experimental autoimmune encephalomyelitis (EAE). The aim of the present study was to investigate the effects of memantine and amantadine on the expression of proinflammatory cytokines such interleukin 1beta (IL-1β), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and various chemokines in the brain of EAE rats. Real-time Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western Blot were used to analyze the cytokine profile. We noticed increased expression of array of cytokines in experimental group when compared to the control. Dramatic increase of IL-1β, IL-6, TNF-α, and chemokines concentration corresponding to the intensity of neurological symptoms and loss of weight was observed in EAE rats. Administration of iGluR antagonists at an advanced stage of unremitting EAE resulted in amelioration of the disease. Cytokine analysis revealed that memantine significantly decreased the expression of interleukins: IL-6 (65%), IL-1β (60%) and TNF-α (45%) whereas treatment with amantadine reduced only the expression of IL-6 (60%) and TNF-α (15%) when compared to EAE animals. These results show that antagonists of iGlu receptors modulate the course of the disease by reducing the expression of proinflammatory cytokines thereby confirming the involvement of glutamate receptors into pathological mechanisms operating during EAE. This study was supported by grant nr NN401620038 from Polish Ministry of Science and Higher Education
17

Involvement of multiple protein kinases in cPLA2 phosphorylation, AA release and cell death in astrocyte treated with 1-methyl-4-phenylpyridinium-the possible key role of PKG

45%
Chalimoniuk M., Stolecka A., Gabryel B., Malecki A., Langfort J.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
Cytosolic phospholipase A2 (cPLA2) demonstrates selective affi nity to arachidonic acid (AA) liberation, which is known to be elevated in PD. We indicated that NO/GC/cGMP pathway was upregulated in the primary astrocyte culture treated with MPP+. We investigated if the cGMP/cGMP-dependent protein kinase (PKG) signaling pathway was involved in 1-methyl-4-phenylpyridinium (MPP+)-induced cPLA2 activation of the primary astrocyte culture. We found increased levels of total and phosphorylated cPLA2 and increased AA release in the primary astrocyte culture exposed to MPP+. We used cPLA2-specifi c inhibitors and Ca2+- independent PLA2 (iPLA2), and we found that cPLA2 released more AA after stimulation with MPP+ than iPLA2 and that there was a time-dependent delay of AA release by iPLA2 compared to cPLA2. The PKG inhibitor KT5823 decreased MPP-induced AA release in the primary astrocyte culture. KT5823, in addition to PKC and ERK1/2 inhibitors, decreased cPLA2 activity as well as total and phosphorylated cPLA2 protein levels in the astrocyte treated with MPP+. Dual treatment with PKG and PKC or ERK1/2 inhibitors had the same effect on cPLA2 activity and protein levels. PKG is involved in the enhancement of cPLA2 phosphorylation at Serine-505 and in AA release in the astrocyte exposed to MPP+. Our results indicate that the nNOS/cGMP/ PKG pathway stimulates cPLA2 phosphorylation at Ser-505 by activation of PKC or ERK1/2. These results suggest that activation of cPLA2 by upregulation nNOS/cGMP pathway may play important role in MPP+-induced astrocyte activation, neurotoxicity and oxidative stress in the nigrostriatal system.
18

Zależne od wieku zmiany biochemiczne i molekularne w mózgu młodych i starych myszy transgenicznych z APP - Tg(Thyl;APP)Va717Ile

45%
Chalimoniuk M., Gasowska M., Cieslik M., Langfort J., Kowalczyk A.
Annals of Warsaw University of Life Sciences - SGGW. Animal Science
|
2011
|
tom 48
19

cGMP-dependent protein kinase is involved in cPLA2 phosphorylation, AA release and cell death in in vivo and in vitro modelsvof 1-methyl-4-phenylpyridinium-induced parkinsonism

39%
Chalimoniuk M., Stolecka A., Zieminska E., Stepien A., Langfort J., Strosznajder J. B.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
We investigated if the cGMP/cCGP-dependent protein kinase (PKG) signaling pathway was involved in 1-methyl-4-phenylpyridinium (MPP+)-induced cPLA2 activation of dopaminergic neuronal cells (PC12 cells). We found increased levels of total and phosphorylated cPLA2 and increased AA release in the nigrostriatal system of MPTPinduced parkinsonism mice and in PC12 cells exposed to MPP+. We used cPLA2-specifi c inhibitors and Ca2+-independent PLA2 (iPLA2), and we found that cPLA2 released more AA after stimulation with MPTP/MPP+ than iPLA2 and that there was a time-dependent delay of AA release by iPLA2 compared to cPLA2. The PKG inhibitor KT5823 decreased MPTP-induced AA release in the nigrostriatal pathway. KT5823, in addition to PKC and ERK1/2 inhibitors, decreased cPLA2 activity as well as total and phosphorlyated cPLA2 protein levels in the midbrain and striatum of MPTP-induced parkinsonism mice. Inhibition occurred within 30 minutes and persisted for up to 24 hours. Similar results were also observed in MPP+-treated PC12 cells. Dual treatment with PKG and PKC inhibitors had the same effect on cPLA2 activity and protein levels. PKG is involved in the enhancement of cPLA2 phosphorylation at Serine-505 and in AA release in PC12 cells exposed to MPP+. In PC12 cells, inhibitors of cPLA2 and PKG increased viability and prevented MPP+-induced apoptosis. Our results indicate that the nNOS/cGMP/PKG pathway stimulates cPLA2 phosphorylation at Ser-505 by activation of PKC or ERK1/2. Our results also suggest that upregulation of the nNOS/cGMP pathway observed in experimental models of PD may mediate dopaminergic neuron degeneration and death through activation of cPLA2. This work was supported by MSHE, Scientifi c Network nr. 28/E32/SN-0053/2007
20
Content available remote

Diversity of endurance training effects on antioxidant defenses and oxidative damage in different brain regions of adolescent male rats

39%
Chalimoniuk M., Jagsz S., Sadowska-Krepa E., Chrapusta S. J., Klapcinska B., Langfort J.
Journal of Physiology and Pharmacology
|
2015
|
tom 66
|
nr 4
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